Arrhythmology

Cardiomyocytes
Heart muscle consists of
three types of cells:

1) Fast cells of working myocardium

that make a contraction as a
response to electric signal created
in pacemaker cells most
common type

2) Slow cells which participate in

conduction through SA and AV
node

3) Pacemaker cells that create the

electric signal.

Connection between two cells is

maintained by desmosomes
Mechanism of cardiomyocyte activity 1
Three cations present in both extra- and intracelular fluid
participate in electrical activity of heart muscle: Na+, K+
and Ca2+. Na+ and Ca2+ are present mainly in ECF (Ca2+
also in endoplasmic reticulum) , K+ in ICF
During fast depolarisation of a cardiomyocyte (phase 0),
voltage-gated sodium channels (INa) open at -65 mV.
Subsequent influx of Na+ leads to depolarisation up to
+40 mV and closing of Na+ channels.
Phase 1 means partial repolarisation carried by diffusion
of K+ through specific ion channels (Ito transient
outward) K+ ions diffuse according to both electrical and
chemical gradient. In the same time, Ca2+ long-lasting
(ICa-L) channels are opened. During phase 0 to 2, heart
muscle cell doesnt respond to any new electrical signal
refractory period
Mechanism of cardiomyocyte activity 2
In phase 2 (plateau), prolonged depolarisation is
maintained by the influx of Ca2+ through ICa-L channels.
Unlike INa or Ito, ICa-L channel is gated both by voltage
and receptor mechanism, that responds to vegetative
nervous signalisation. Ca2+ binds to ryanodin receptor of
sarcoplasmic reticulum, where it enhances the release of
more Ca2+ into the cytoplasm. Ca2+ then binds troponin
which changes its conformation and stops blocking the
actin-myosin interaction. Contraction of muscle fibre
follows as in other types of muscles. Another, delayed
K+ channel (IK) is open.
Finally, with closing of Ca2+ channel, efflux of K+ lowers
the voltage inside the cardiomyocyte to the values during
diastole (phase 3)
Before next repolarisation, Na+ ions are pumped outside
the cell in exchange for K+ by Na/K ATP-ase (3:2). Some
Na+ ions return inside the cell in change for Ca2+ through
specific exchanger Ca2+ is also pumped into
sarcoplasmic reticulum.The heart muscle gets to diastole
 Pacemaker cells
In pacemaker cells, sympathicus- and parasympathicus-
controlled sodium, potassium and calcium channels remain
open during the diastole, leading into continual loss of
negative voltage up to -65mV, when fast depolarisation
begins.
Pacemaker cells are present in SA node, AV node and
Purkinje fibres
 Normal conduction within the heart
According to Katzung's Basic & Clinical Pharmacology.
McGraw-Hill Medical; 9 edition (December 15, 2003)
Aorta

M /1
SA node
VC

Atrial myocardium

AV node 1

SA node
Bundle of His

AV node Purk. fibre

ventricle
Bundle of His

ECG T
P
U

QRS
Time (s)
Purkinje fibre
0.2 0.4 0.6
 Sinoatrial (SA) node
Group of pacemaker cells located in the right atrium
Under normal circumstances it serves as primary
pacemaker of the heart
It spontaneously generates electrical impulses at a
rate of 60-90/min
The SA node is richly
innervated by both sympaticus
and parasympaticus, which
modify the SA node rate and
thus heart frequency
 Atrial conduction system
Bachmanns bundle conducts action potentials
to the left atrium
Internodal tracts (anterior, middle and posterior)
run from SA node to AV node, converging near
the coronary sinus. Atrial automacity foci are
present within the atrial conduction system
 Atrioventricular (AV) node
Area of specialized tissue located between atria and ventricles, near the
coronary sinus and tricuspid valve. It serves as secondary pacemaker and is
the only way of electric connection between the atria and the ventricles
under normal circumstances.
AV node consists of 3 zones: AN (atria-nodus), N (nodus) and NH (nodus-
His).
In AN zone, the conduction gets slower, as there is less sodium channels
and slower depolarisation
N zone is formed by nodal cells with low voltage (-50mV) slow cells.
These cells do not contain sodium channels, their depolarisation is then
mediated by Ca2+. The conduction delays by about 0,12s there. The Ca2+ ICa-
L receptors are influenced by the sympathicus and the parasympathicus.
In NH zone, the nuber of sodium
channels increase again. The cells of
NH zone can take over the function
of pacemaker, in the case if no signal from
upper parts of the conduction system is
present. Its rate is slower than that
of SA node: 40-60/min
 Bundle of His
Part of cardiac tissue specialized for fast electrical
conduction that leads the signal from AV-node to
working myocardium of the ventricles.
After its short course, the Bundle of His branches ito
right and left bundle branch (Tawara branches). Right
bundle branch is long and thin, thus more vulnerable
than the left one
Left bundle branch is then
divided into the left
anterior and left posterior
fascicle
 Purkinje fibres
Terminal part of the conduction system
Tertiary pacemaker idioventricular rhythm (20-40/min), without
innervation

Jan Evangelista Purkyn (1787-1869),

Czech physiologist
 12-leads ECG (uses 10 electrodes)
Electrode placement:
RA: On the right arm, avoiding bony prominences.
LA: In the same location that RA was placed, but on the left arm this time.
RL: On the right leg, avoiding bony prominences.
LL: In the same location that RL was placed, but on the left leg this time.
V1: In the fourth intercostal space (between ribs 4 & 5) just to the right of the
sternum (breastbone).
V2: In the fourth intercostal space (between ribs 4 & 5) just to the left of the
sternum.
V3: Between leads V2 and V4.
V4: In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line
(the imaginary line that extends down from the midpoint of the clavicle
(collarbone).
V5: Horizontally even with V4, but in the anterior axillary line. (The anterior
axillary line is the imaginary line that runs down from the point midway between
the middle of the clavicle and the lateral end of the clavicle; the lateral end of
the collarbone is the end closer to the arm.)
V6: Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary
line is the imaginary line that extends down from the middle of the patients
armpit.)
12-leads ECG electrode placement
Evaluation of electrical signal:
Eindhovens triangle
Normal ECG curve
 Normal Sinus Rhythm

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Implies normal sequence of conduction, originating in the sinus node and

proceeding to the ventricles via the AV node and His-Purkinje system.

EKG Characteristics: Regular narrow-complex rhythm

Rate 60-100 bpm
Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead aVR
 Description of ECG
rhythm action
sinus regular
60-90/min irregular
other
junctional frequency
40-60/min normal
idioventricular 60 90/min
30-40/min tachycardia
atrial fibrilation >90/min
atrial flutter bradycardia
<60/min
description of waves and intervals
electrical axis of the heart
 Arrhythmias:

Electrophysiological abnormalities arising from the

impairment of the impulse
1. genesis (origin), 2. conduction, 3. both previous
Arrhythmias are defined by exclusion - i.e., any rhythm that is not
a normal sinus rhythm (NSR, 60-100 bpm) is an arrhythmia

With respect to the

Frequency bradyarrythmias vs. tachyarrhythmias
Localization supraventricular (SV), ventricular (V)
Mechanism early after depolarisation (EAD), delayed after
depolarisation (DAD), re-entry
 Mechanism of Arrhythmia
Abnormal heart pulse formation
1. Sinus pulse
2. Ectopic pulse
3. Triggered activity
Abnormal heart pulse
conduction
1. Reentry
2. Conduct block
 Possible causes of arrhytmia
Vegetative nervous system disorder (nervous lability, compensation of heart failure,
shock, anxiety)

Ischaemia, hypoxia and reperfusion, pH disorders

Disorders of iont balance

Disorders of myocardium hypertrophy, dilatation, amyloidosis, scar aftar acute

myoacrdial infarction

Inflammation

Drugs (-blockers, digitalis, antiarrhytmics)

General state (trauma, endokrinopathy..)

Genetic causes (ion channel mutations)

Aberrant conduction bundle of KENT (WPW syndrom aberrant track between the
atria and the ventricles bypassing the AV-node
 Brady- and tachyarrhythmias:
1. Bradyarrhythmias
- SA block
- sick-sinus syndrome
- AV block

2. Tachyarrhythmias
a) Supraventricular (SV)
- SV extrasystoles atrial, junction
- atrial tachycardia, flutter, fibrillation
- AV node re-entry tachycardia (AVNRT)
- AV re-entry tachycardia (Wolf-Parkinson-White syndrome)
b) Ventricular
- ventricular extrasystoles
- ventricular tachycardia
- flutter/fibrillation
Badyarrhythmias
Recognizing altered automaticity on EKG

Gradual onset and termination of the arrhythmia.

The P wave of the first beat of the arrhythmia is

typically the same as the remaining beats of the
arrhythmia (if a P wave is present at all).
Decreased Automaticity

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Sinus Bradycardia
 Sinus Bradycardia

HR< 60 bpm; every QRS narrow, preceded by p wave

Can be normal in well-conditioned athletes
HR can be<30 bpm in children, young adults during
sleep, with up to 2 sec pauses
 Sinus bradycardia - etiologies

Normal aging
15-25% Acute MI, esp. affecting inferior wall
Hypothyroidism, infiltrative diseases
(sarcoid, amyloid)
Hypothermia, hypokalemia
SLE, collagen vasc diseases
Situational: micturation, coughing
Drugs: beta-blockers, digitalis, calcium channel
blockers, amiodarone, cimetidine, lithium
Increased/Abnormal Automaticity

Sinus tachycardia

Ectopic atrial tachycardia

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Junctional tachycardia
Sinus tachycardia - etiologies
Fever Hypotension and shock
Hyperthyroidism Pulmonary embolism
Effective volume Acute coronary ischemia
depletion and myocardial infarction
Anxiety Heart failure
Pheochromocytoma Chronic pulmonary
Sepsis disease
Anemia Hypoxia
Exposure to stimulants
(nicotine, caffeine) or illicit
drugs
 Sinus Arrhythmia

Variations in the cycle lengths between p waves/ QRS

complexes
Will often sound irregular on exam
Normal p waves, PR interval, normal, narrow QRS
 Sinus arrhythmia
Usually respiratory--Increase in heart rate during
inspiration
Exaggerated in children, young adults and
athletesdecreases with age
Usually asymptomatic, no treatment or referral
Can be non-respiratory, often in normal or
diseased heart, seen in digitalis toxicity
Referral may be necessary if not clearly
respiratory, history of heart disease
 Sick Sinus Syndrome

All result in bradycardia

Sinus bradycardia (rate of ~43 bpm) with a sinus pause
Often result of tachy-brady syndrome: where a burst of
atrial tachycardia (such as afib) is then followed by a
long, symptomatic sinus pause/arrest, with no
breakthrough junctional rhythm.
Sick Sinus Syndrome - etiology
Often due to sinus node fibrosis, SNode arterial
atherosclerosis, inflammation (Rheumatic fever,
amyloid, sarcoid)
Occurs in congenital and acquired heart disease
and after surgery
Hypothyroidism, hypothermia
Drugs: digitalis, lithium, cimetidine, methyldopa,
reserpine, clonidine, amiodarone
Most patients are elderly, may or may not have
symptoms
 Triggered activity
Long QT a bradycardia
2. Delayed afterdepolarization (DAD)
Mechanism of Reentry
Mechanism of Reentry
 Reentrant Rhythms
AV nodal reentrant tachycardia (AVNRT)
AV reentrant tachycardia (AVRT)
Orthodromic
Antidromic
Atrial flutter
Atrial fibrillation
Ventricular tachycardia
 Recognizing reentry on EKG

Abrupt onset and termination of the arrhythmia.

The P wave of the first beat of the arrhythmia is

different from the remaining beats of the
arrhythmia (if a P wave is present at all).
Example of AVNRT
Mechanism of AVNRT
 Atrial Flutter

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Most cases of atrial flutter are caused by a large reentrant circuit in the wall of the
right atrium

EKG Characteristics: Biphasic sawtooth flutter waves at a rate of ~ 300 bpm

Flutter waves have constant amplitude, duration, and
morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node,
resulting in ventricular rates of either 150 or 75
bpm
 Unmasking of Flutter Waves

Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005.

In the presence of 2:1 AV block, the flutter waves may not

be immediately apparent. These can be brought out by
administration of adenosine.
 Atrial Fibrillation

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Atrial fibrillation is caused by numerous wavelets of depolarization spreading
throughout the atria simultaneously, leading to an absence of coordinated
atrial contraction.
This kind of rhythm is present in up to 5% of adult population, mostly in older
age. It is often connected with other diseases of the heart (ischaemic haert
disease, heart failure.
Atrial fibrillation is important because it can lead to:
Hemodynamic compromise
Systemic embolization
Symptoms
 Atrial Fibrillation

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ECG Characteristics: Absent P waves

Presence of fine fibrillatory waves which vary in
amplitude and morphology
Irregularly irregular ventricular response
Ventricular arrhythmia
Ventricular extrasystoles (VES)
Is caused by either reentrant signaling or
enhanced automaticity in some ectopic focus

The QRS complex is enlarged (>120ms) and

has different shape
 Coupling of VES
Premature ventricular beats occurring after every normal beat are
termed ventricular bigeminy, if 2 normal QRS complexes are folloved
by VES, we speak of ventricular trigeminy.

Two VES grouped together are called a couplet, three a triplet. Runs
longer than 3 VES is referred as ventricular tachycardia
 What is this arrhythmia?

Ventricular tachycardia

Ventricular tachycardia is usually caused by reentry, and most

commonly seen in patients following myocardial infarction.
Polymorphic ventricular tachycardia
torsades de pointes
Is connected with prolonged QT interval.
The place of origin of the beats is moving that
leads into different shape of QRS
Ventricular fibrillation (lethal
condition)
Conduction Block
 Rhythms Produced by Conduction
Block

AV Block (relatively common)

1st degree AV block
Type 1 2nd degree AV block
Type 2 2nd degree AV block
3rd degree AV block

SA Block (relatively rare)

 Atrioventricular Block
AV block is a delay or failure in
transmission of the cardiac impulse
from atrium to ventricle.
Etiology:
Atherosclerotic heart disease;
myocarditis; rheumatic fever;
cardiomyopathy; drug toxicity;
electrolyte disturbance, collagen disease,
levs disease.
 1st Degree AV Block

The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

ECG Characteristics: Prolongation of the PR interval, which is constant

All P waves are conducted
 2nd Degree AV Block
Type 1
(Wenckebach)

EKG Characteristics: Progressive prolongation of the PR interval until a P

wave is not conducted.
As the PR interval prolongs, the RR interval actually
shortens

Type 2

EKG Characteristics: Constant PR interval with intermittent failure to conduct

 3rd Degree (Complete) AV Block

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EKG Characteristics: No relationship between P waves and QRS complexes

Relatively constant PP intervals and RR intervals
Greater number of P waves than QRS complexes
 SA arrest with compensatory AV activity

When the activity of SA node is stopped, AV node takes over the role of
pacemaker.
Very similar type of arrhythmia is SA block: Pacing in SA node is generated, but
not conducted to the myocardium+
 Intraventricular Block
Intraventricular conduction system:
1. Right bundle branch
2. Left bundle branch
3. Left anterior fascicular
4. Left posterior fascicular
 Intraventricular Block
Etiology:
Myocarditis, valve disease,
cardiomyopathy, CAD, hypertension,
pulmonary heart disease, drug toxicity,
Lenegre disease, Levs disease et al.
Manifestation:
Single fascicular or bifascicular block is
asymptom; tri-fascicular block may
have dizziness; palpitation, syncope
and Adams-stokes syndrome
 Premature contractions
The term premature contractions
are used to describe non sinus beats.
Common arrhythmia
The morbidity rate is 3-5%
Atrial premature contractions
(APCs)
APCs arising from somewhere in either the
left or the right atrium.
Causes: rheumatic heart disease, CAD,
hypertension, hyperthyroidism,
hypokalemia
Symptoms: many patients have no
symptom, some have palpitation, chest
incomfortable.
Therapy: Neednt therapy in the patients
without heart disease. Can be treated with
-blocker, propafenone, moricizine or
verapamil.
 Ventricular Premature
Contractions (VPCs)
Etiology:
1. Occur in normal person
2. Myocarditis, CAD, valve heart disease,
hyperthyroidism, Drug toxicity
(digoxin, quinidine and anti-anxiety
drug)
3. electrolyte disturbance, anxiety,
drinking, coffee
 Pre-excitation syndrome
(W-P-W syndrome)
There are several type of accessory
pathway
1. Kent: adjacent atrial and ventricular
2. James: adjacent atrial and his
bundle
3. Mahaim: adjacent lower part of the
AVN and ventricular
Usually no structure heart disease,
occur in any age individual
 WPW syndrome

Manifestation:
Palpitation, syncope, dizziness
Arrhythmia: 80% tachycardia is
AVRT, 15-30% is AFi, 5% is AF,
May induce ventricular fibrillation
Wolff-Parkinson White Syndrome (WPW) is a condition
in which the heart beats too fast due to abnormal, extra
electrical pathways between the hearts atrium and
ventriculum .
Thank you for your attention